Herring Neil, Paterson David J
Burdon Sanderson Cardiac Science Centre, Department of Physiology, Anatomy and Genetics, Parks Road, Oxford OX1 3PT, UK.
Exp Physiol. 2009 Jan;94(1):46-53. doi: 10.1113/expphysiol.2008.044776. Epub 2008 Oct 22.
The traditional model of efferent cardiac noradrenaline and acetylcholine release being driven solely via brainstem integration of circulatory reflex afferent input needs to be modified in the light of the discovery of numerous local cardiac factors that impact on peripheral neuronal neurotransmitter release. These neuromodulators can be intrinsic to sympathetic ganglia or vagal neurons (such as neuronal nitric oxide synthase), act as cotransmitters between these neuronal populations (such as neuropeptide Y) or are released from the myocardium itself to act on neurons in a paracrine manner (such as natriuretic peptides). Both myocardial infarction and congestive heart failure are characterized by enhanced regulation of these neuromodulators. This review will focus on recent evidence that nitric oxide, natriuretic peptides and neuropeptide Y act by converging on neuronal cyclic nucleotide-dependent pathways to alter the autonomic phenotype in both health and disease.
鉴于发现了众多影响外周神经元神经递质释放的局部心脏因子，传统的传出性心脏去甲肾上腺素和乙酰胆碱释放仅通过脑干整合循环反射传入输入来驱动的模型需要修正。这些神经调节剂可以是交感神经节或迷走神经元固有的（如神经元型一氧化氮合酶），作为这些神经元群体之间的共递质（如神经肽Y），或者从心肌本身释放出来以旁分泌方式作用于神经元（如利钠肽）。心肌梗死和充血性心力衰竭都以这些神经调节剂的调节增强为特征。本综述将聚焦于近期的证据，即一氧化氮、利钠肽和神经肽Y通过汇聚于神经元环核苷酸依赖性途径来改变健康和疾病状态下的自主神经表型。
